Evidence map›Paper›PMID 36194627›Full record

ArticleEMBO reports2022

NLRP3 activation in neutrophils induces lethal autoinflammation, liver inflammation, and fibrosis.

Benedikt Kaufmann, Aleksandra Leszczynska, Agustina Reca, Laela M Booshehri, Janset Onyuru, ZheHao Tan, Alexander Wree, Helmut Friess, Daniel Hartmann, Bettina Papouchado and 5 more

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  10. The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Article
  12. Article
  13. Liver transplant-facilitated CD161Nature communications · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Purinergic Signaling in Non-Parenchymal Liver Cells.International journal of molecular sciences · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Benedikt KaufmannDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Aleksandra LeszczynskaDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Agustina RecaDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Laela M BooshehriDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Janset OnyuruDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.ORCID 0000-0003-3924-8487
ZheHao TanDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Alexander WreeDepartment of Hepatology and Gastroenterology, Charité, Universitätsmedizin Berlin, Berlin, Germany.
Helmut FriessDepartment of Surgery, TUM School of Medicine, Klinikum rechts der Isar, Technical, University of Munich, Munich, Germany.
Daniel HartmannDepartment of Surgery, TUM School of Medicine, Klinikum rechts der Isar, Technical, University of Munich, Munich, Germany.
Bettina PapouchadoDepartment of Pathology, University of California San Diego, La Jolla, California, USA.
Lori BroderickDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Hal M HoffmanDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Ben A CrokerDepartment of Pediatrics, University of California San Diego, La Jolla, California, USA.
Yanfang Peipei Zhu *Department of Pediatrics, University of California San Diego, La Jolla, California, USA.
Ariel E Feldstein *Department of Pediatrics, University of California San Diego, La Jolla, California, USA.ORCID 0000-0001-7202-3840
University of California San Diego · USTUM Klinikum · DECharité - Universitätsmedizin Berlin · DE

Funding

Neutrophil Survival and Demise During Inflammatory StatesP01HL152958 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI CATZ, SERGIO DANIEL · 2021 to 2025
$12.4M
Vesicular trafficking mechanisms regulating granulocyte functionR01HL088256 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI Sergio Daniel Catz · 2009 to 2026
$9.0M
Sterile inflammation and pyroptotic cell death in liver fibrosisR01DK113592 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Ariel Feldstein, HAROLD M HOFFMAN · 2017 to 2026
$4.8M
Defining the roles of RIPK1 and RIPK3 in emergency hematopoiesisR01HL124209 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CROKER, BEN ADAM · 2015 to 2019
$2.2M
Gain of function mutations in inflammasome related genes in human and experimental alcoholic liver diseaseR01AA024206 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDSTEIN, ARIEL · 2019 to 2021
$988k
NHLBI NIH HHS P01 HL152958NHLBI NIH HHS R01 HL088256NHLBI NIH HHS R01 HL124209NIAAA NIH HHS R01 AA024206NIDDK NIH HHS R01 DK113592
6 · The paper itself

Abstract

Sterile inflammation is a central element in liver diseases. The immune response following injurious stimuli involves hepatic infiltration of neutrophils and monocytes. Neutrophils are major effectors of liver inflammation, rapidly recruited to sites of inflammation, and can augment the recruitment of other leukocytes. The NLRP3 inflammasome has been increasingly implicated in severe liver inflammation, fibrosis, and cell death. In this study, the role of NLRP3 activation in neutrophils during liver inflammation and fibrosis was investigated. Mouse models with neutrophil-specific expression of mutant NLRP3 were developed. Mutant mice develop severe liver inflammation and lethal autoinflammation phenocopying mice with a systemic expression of mutant NLRP3. NLRP3 activation in neutrophils leads to a pro-inflammatory cytokine and chemokine profile in the liver, infiltration by neutrophils and macrophages, and an increase in cell death. Furthermore, mutant mice develop liver fibrosis associated with increased expression of pro-fibrogenic genes. Taken together, the present work demonstrates how neutrophils, driven by the NLRP3 inflammasome, coordinate other inflammatory myeloid cells in the liver, and propagate the inflammatory response in the context of inflammation-driven fibrosis.

Indexed as

HepatitisInflammasomesAnimalsFibrosisInflammationInterleukin-1betaMiceNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousefibrosisliver inflammationmacrophageneutrophilNLR Family Pyrin Domain Containing 3

Identifiers

PMID36194627
PMCPMC9638850
OpenAlexW4301181048

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.